Fluticasone-associated cutaneous allergic granulomatous vasculitis: an underrecognized but important cause of drug-induced cutaneous Churg-Strauss syndrome

Allergic granulomatous vasculitis, or Churg-Strauss syndrome, is a small vessel, multisystem vasculitis that can affect multiple organs. It is usually idiopathic, but recent case reports have implicated leukotriene receptor antagonists (LTRA) and inhaled corticosteroids in the development of this rare syndrome. We report a case that acutely developed skin-limited Churg Strauss-like cutaneous allergic granulomatous vasculitis after initiating therapy with inhaled fluticasone and salmeterol for poorly controlled asthma symptoms. Our result thus highlights the importance of keeping the differential diagnosis of drug-induced Churg-Strauss syndrome in patients who have recently been prescribed inhaled steroids like fluticasone when they present with rashes of varying severity.     

Vancomycin-induced acute granulomatous interstitial nephritis: therapeutic options

Drug-induced acute renal failure is a commonly encountered mode of renal injury in the hospitalized patient. Vancomycin is a frequently used antibiotic in patients with Gram-positive bacterial infections. In the present study, we evaluated an index case of a patient who developed severe acute granulomatous interstitial nephritis and provided a review of the reported cases of vancomycin-induced acute renal failure in the literature. A Medline search revealed a total of 11 cases of vancomycin-induced interstitial nephritis. In 2 reported cases, interstitial nephritis has been reported with associated granuloma formation. However, the role of T cells in the formation of interstitial nephritis and in the choice of therapeutic modalities in this scenario has not been evaluated in the past. In the index case, we have evaluated the effect of treatment on the basis of the type of cellular infiltrates and provided a follow-up by carrying out the repeat biopsy.     

The LeFort I transmaxillary approach to skull base tumors

This article discusses the surgical approach using the LeFort I and its variations to the extracranial skull base for removal of craniocervical lesions from the sphenoid to the fourth cervical vertebra between the carotids. Clival lesions with superior and inferior extension and nasopharyngeal lesions can be accessed by this approach. The outcome of surgical, radiation, and chemotherapeutic treatment is beyond the scope of this brief article, which focuses on the technical aspects of cranial base tumor exposure.     

Daunorubicin induced Stevens‐Johnson syndrome: A case report

Clinicians should consider the possible association of Daunorubicin with Stevens‐Johnson syndrome (SJS), administer it with caution and promptly evaluate all subsequently developing cutaneous reactions with a high index of suspicion for Stevens‐Johnson syndrome.     

Ethanol and Vitamin D Receptor in T Cell Apoptosis

Ethanol has been demonstrated to cause T cell apoptosis. In the present study, we evaluated the role of VDR and the renin angiotensin system (RAS) in oxidative stress-induced T cell apoptosis. Ethanol-treated human T cells displayed down regulation of vitamin D receptor (VDR) and the activation of the RAS in the form of enhanced T cell renin expression and angiotensin II (Ang II) production. The silencing of VDR with siRNA displayed the activation of the RAS, and activation of the VDR resulted in the down regulation of the RAS. It suggested that ethanol-induced T cell RAS activation was dependent on the VDR status. T cell ROS generation by ethanol was found to be dose dependent. Conversely, ethanol-induced ROS generation was inhibited if VDR was activated or Ang II was blocked by an angiotensin II type 1 (AT1) receptor blocker (Losartan). Furthermore, it was observed that ethanol not only induced double strand breaks in T cells but also attenuated DNA repair response, whereas, VDR activation inhibited ethanol-induced double strand breaks and also enhanced DNA repairs. Since free radical scavengers inhibited ethanol-induced DNA damage, it would indicate that ethanol-induced DNA damage was mediated through ROS generation. These findings indicated that ethanol-induced T cell apoptosis was mediated through ROS generation in response to ethanol-induced down regulation of VDR and associated activation of the RAS.     

A Role for Extracellular Vesicles in SARS-CoV-2 Therapeutics and Prevention

Extracellular vesicles (EVs) are the common designation for ectosomes, microparticles and microvesicles serving dominant roles in intercellular communication. Both viable and dying cells release EVs to the extracellular environment for transfer of cell, immune and infectious materials. Defined morphologically as lipid bi-layered structures EVs show molecular, biochemical, distribution, and entry mechanisms similar to viruses within cells and tissues. In recent years their functional capacities have been harnessed to deliver biomolecules and drugs and immunological agents to specific cells and organs of interest or disease. Interest in EVs as putative vaccines or drug delivery vehicles are substantial. The vesicles have properties of receptors nanoassembly on their surface. EVs can interact with specific immunocytes that include antigen presenting cells (dendritic cells and other mononuclear phagocytes) to elicit immune responses or affect tissue and cellular homeostasis or disease. Due to potential advantages like biocompatibility, biodegradation and efficient immune activation, EVs have gained attraction for the development of treatment or a vaccine system against the severe acute respiratory syndrome coronavirus 2 (SARS CoV-2) infection. In this review efforts to use EVs to contain SARS CoV-2 and affect the current viral pandemic are discussed. An emphasis is made on mesenchymal stem cell derived EVs’ as a vaccine candidate delivery system.

Graphical Abstract

     

Presumed multifocal cryptococcol choroidopathy prior to specific systemic manifestation

Purpose: Disseminated cryptococcosis is a major cause of morbidity and mortality in immunocompromised individuals, especially those with the acquired immunodeficiency syndrome (AIDS). Early diagnosis and treatment greatly improves the outcome, so clinical clues that lead to prompt diagnosis are important. Methods: Three patients with AIDS in whom multifocal choroiditis and choroidal lesions were the initial signs of disseminated cryptococcosis were treated with systemic amphotericin B and flucytosine. All of the patients had a systemic work-up that included evaluation of the cerebral spinal fluid (CSF). Results: All three patients who were seen with the choroidal lesions as the presenting sign were noted to have either positive titers for cryptococcus or cultures that grew cryptococcus in the CSF. The choroidal lesions are presumed to be due to cryptococcus as no histopathologic or microscopic studies were available for ocular tissues. The choroidal lesions started to resolve one to three months after systemic treatment with amphotericin B and flucytosine. Conclusion: Primary choroidal lesions in patients with AIDS may herald severe systemic disseminated disease. Funduscopic examination, however, may detect disseminated cryptococcal disease before other overt clinical manifestations, thereby allowing prompt institution of effective therapy. This revised version was published online in September 2006 with corrections to the Cover Date.